High impact information on Arid3a

• This B-cell specific protein, termed Bright (B cell regulator of IgH transcription), is found in both soluble and matrix insoluble nuclear fractions [1].
• Our study also revealed that recombinant marine (rm)IL-2 and rmIL-7 reciprocally induced high expressions of IL-7R and IL-2R, respectively, on gamma delta (Dim) T cells but not on gamma delta (Bright) cells [2].
• Our earlier reports demonstrated that Bright coimmunoprecipitates with Bruton's tyrosine kinase (Btk) and that these proteins associate in a DNA-binding complex in primary B cells [3].
• In order to determine if Btk is important for Bright function, a transcription activation assay was established and analyzed using real-time PCR technology [3].
• Cux/CDP antagonizes the effects of the Bright transcription activator at both the DNA binding and functional levels [4].

Biological context of Arid3a

• Immunoglobulin gene transcription was enhanced when Bright and Btk were coexpressed [3].
• Bright activation results in up-regulation of mu transcription; however, it is not clear whether Bright function is critical for normal B cell development [5].
• We expected to find Bright expression in a subset of mature spleen cells, but also observed Bright in a subset of normal B lymphocytic progenitors in both adult bone marrow (BM) and in fetal liver as early as day 12 of gestation [6].
• In this study, we have used transgenic animals to test the functional importance of a 5' portion of the VH1 promoter which is known to contain a matrix attachment region as well as binding sites for the negative regulator NF-microNR and Bright, a protein complex which is induced upon stimulation of B cells with IL-5 and antigen [7].

Anatomical context of Arid3a

• In addition, new splice variants of Bright were observed in fetal tissues [6].
• Thus, Bright expression is highly regulated in normal murine lymphocytes and occurs both early and late during B cell differentiation [6].

Regulatory relationships of Arid3a

• Thus, the ability of Bright to enhance immunoglobulin transcription critically requires functional Btk [3].

Other interactions of Arid3a

• B cells from immunodeficient mice with a mutation in Btk failed to produce stable Bright DNA-binding complexes [3].

Analytical, diagnostic and therapeutic context of Arid3a

• Furthermore, we observed Btk in the nucleus of activated murine B cells, and mobility shift assays suggest that it is a component of the Bright DNA-binding complex [8].
• The gamma delta T cells express low levels of IL-2R and IL-7R as shown by flow cytometry and reverse transcriptase-PCR analysis, whereas gamma delta (Bright) T cells did not express either receptor [2].

References